The vascular endothelium represents a critical interface between blood and all tissues. Endothelial dysfunction contributes to the development of both acute inflammatory disease states, such as endotoxemia and sepsis, and chronic inflammatory disease states, such as atherosclerosis, diabetes, rheumatoid arthritis, and inflammatory bowel disease (Aird, Blood 101:3765-3777, 2003; Aird, Lancet 365:63-78, 2007; Baker et al., Cell Metab. 13:11-22, 2011; Gareus et al., Cell Metab. 8:372-383, 2008; Guerci et al., Diabetes Metab. 27:436-477, 2001; Hansson and Libby, Nat. Rev. Immunol. 6:508-519, 2006; Khan et al., Nat. Rev. Rheumatol. 6: 253-261, 2010; Roifman et al., Clin. Gastroenterol. Hepatol. 7:175-182, 2009). In response to inflammatory stimuli, the vascular endothelium expresses a number of adhesion molecules that play key roles in the recruitment of leukocytes to sites of inflammation (Ley et al., Nat. Rev. Immunol. 7:678-689, 2007; Pober and Sessa, J. Immunol. 138:3319-3324, 2007). In particular, vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and intercellular adhesion molecule 1 (ICAM-1) mediate early leukocyte attachment and rolling events. An inflammatory response within tissues is subsequently generated after events such as firm adhesion and transmigration occur (Ley et al., Nat. Rev. Immunol. 7:678-689, 2007). Clinical studies have found that the soluble forms of these adhesion molecules are increased in patients experiencing vascular inflammatory disease (Shapiro et al., Crit. Care 14:R182, 2010; Xu et al., Int. J. Cardiol. 64:253-258, 1998).